{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T23:06:50Z","timestamp":1777417610523,"version":"3.51.4"},"reference-count":67,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T00:00:00Z","timestamp":1768348800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Obesity represents a global health concern, with the hypothalamus playing a central role in regulating energy balance. Chlorpyrifos (CPF), a widely used organophosphate pesticide, is now recognized as an endocrine-disrupting chemical (EDC). Although the peripheral metabolic effects of CPF are relatively well characterized, its potential impact on central energy balance remains to be investigated. Here, we examined, both\n                      <jats:italic>in vitro<\/jats:italic>\n                      in murine hypothalamic cells and\n                      <jats:italic>in vivo<\/jats:italic>\n                      in murine hypothalami, whether CPF modulates the orexigenic mediators Neuropeptide Y (Npy) and Agouti-related peptide (Agrp). We further explored the molecular mechanisms underlying this regulation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      For\n                      <jats:italic>in vitro<\/jats:italic>\n                      studies, murine mHypoE-N46 hypothalamic cells were treated with CPF (1 pM) under acute (4 h) and chronic (6-day) exposure conditions. For\n                      <jats:italic>in vivo<\/jats:italic>\n                      studies, hypothalamic tissue from CD-1 mice chronically exposed to CPF (10 mg\/kg\/day), from conception to 6 months of age while maintained on a standard diet, were analyzed. Gene and protein expression levels, as well as neuropeptide secretion, were assessed by qPCR, Western blotting, and ELISA, respectively. Selective pharmacological antagonists of ER\u03b2 and ER\u03b1 were employed to determine receptor-specific effects.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Both acute and chronic CPF exposure significantly increased\n                      <jats:italic>Npy<\/jats:italic>\n                      and\n                      <jats:italic>Agrp<\/jats:italic>\n                      mRNA expression and secretion in mHypoE-N46 cells. Chronic CPF treatment selectively upregulated\n                      <jats:italic>ER\u03b2<\/jats:italic>\n                      at the mRNA and protein levels, whereas\n                      <jats:italic>ER\u03b1<\/jats:italic>\n                      was unaffected. Pharmacological inhibition confirmed ER\u03b2 as the main mediator of CPF action. Consistently,\n                      <jats:italic>in vivo<\/jats:italic>\n                      hypothalamic samples from CPF-exposed mice displayed increased\n                      <jats:italic>Npy<\/jats:italic>\n                      and\n                      <jats:italic>Agrp<\/jats:italic>\n                      expression and an elevated\n                      <jats:italic>ER\u03b2\/ER\u03b1<\/jats:italic>\n                      ratio, mirroring the\n                      <jats:italic>in vitro<\/jats:italic>\n                      findings. Also, CPF exposure increased\n                      <jats:italic>leptin receptor<\/jats:italic>\n                      (\n                      <jats:italic>Lepr<\/jats:italic>\n                      ) expression both\n                      <jats:italic>in vitro<\/jats:italic>\n                      and\n                      <jats:italic>in vivo<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our findings indicate that CPF acts as a central endocrine disruptor by shifting estrogen receptor signaling toward ER\u03b2 dominance, thereby promoting orexigenic neuropeptide expression. Together with the increased\n                      <jats:italic>Lepr<\/jats:italic>\n                      expression, this mechanism may contribute to hypothalamic dysfunction and metabolic imbalance. The evolutionary conservation of hypothalamic circuits suggests that similar mechanisms may operate across species and impact metabolic health.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fendo.2025.1726498","type":"journal-article","created":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T05:16:03Z","timestamp":1768367763000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["The endocrine disruptor chlorpyrifos alters hypothalamic Npy and Agrp expression via ER\u03b2-dependent regulation in vitro and in vivo"],"prefix":"10.3389","volume":"16","author":[{"given":"Monica","family":"Pastorino","sequence":"first","affiliation":[{"name":"Department of Translational Medicine, Federico II University of Naples","place":["Naples, 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